Folliculitis decalvans

[1]

Meet the patient

A 34-year-old man has spent eighteen months watching the crown of his scalp "melt". Crops of tender yellow pustules erupt over the vertex and occiput, crust over, and leave behind smooth, shiny, hairless skin. His GP has prescribed four courses of oral flucloxacillin; each time the pustules settle for a fortnight, then roar back. Today, without a dermatoscope, you can see clusters of a dozen hairs emerging from single dilated openings — tufts, ringed by an angry erythematous rim.[1][4]

Two exam questions are now live, and they are the two that decide every case of cicatricial alopecia: is this neutrophilic or lymphocytic? (look for the pus) and what is the first-line regimen, and why must it never be given alone? Hold those two questions and everything below slots into place.[1][2]

The disease in one breath — Quinquaud's tufts and pus

Folliculitis decalvans is a neutrophilic, follicle-rupturing, scarring alopecia — and its three definitional pillars are the only opening a viva needs.[1]

Etymology for viva gold: Quinquaud disease, after Paul Quinquaud, who described it in Paris in 1888 — older than most of the antibiotics we now use to treat it. Capillitii, the epithet sometimes appended, is Latin for "of the scalp hair". Both names survive because the clinical picture they name is unmistakable.[3]

The three pillars, in the order examiners want them:[1]

1. Neutrophilic, not lymphocytic — the destructive infiltrate around the follicle is dominated by neutrophils, which seats FD squarely in the neutrophilic subgroup of the primary cicatricial alopecias and separates it at a stroke from lichen planopilaris, frontal fibrosing alopecia, central centrifugal cicatricial alopecia, and discoid lupus.[2][4]
2. Tufted folliculitis is pathognomonic — 5 to 20 hair shafts emerging from a single dilated follicular opening (the doll's hair sign), produced when inflammation fuses the walls of adjacent follicles into one common infundibulum.[3]
3. S. aureus in roughly 70% of cultures, but not a simple pyoderma — the organism triggers an abnormal, persistent neutrophilic response (superantigens, biofilm) that outlives the bacterium. That is why a short course of flucloxacillin predictably fails, and why the scarring is permanent.[1][8]

[1] [1]

Neutrophilic or lymphocytic? — the cicatricial split that owns the viva

The single most powerful fork in scarring alopecia is the cell on the biopsy: pus points one way, perifollicular scale and erythema point the other. Everything — the differential, the biopsy site, the drug choice — hangs off it.[2][4]

The working classification of primary cicatricial alopecias, sorted by the dominant inflammatory cell, is examinable because it is the lens through which every scarring alopecia is read:[2]

[1]

The one-line discriminator: pus = neutrophilic; no pus = lymphocytic. Hold that line and you will never biopsy the wrong zone or reach for the wrong drug class.[2]

Within FD itself, the disease runs through three temporal stages — the same illness at three points on the clock.[1][7]

1. Early / papulopustular. Discrete follicular papules and yellow pustules on an erythematous base over vertex and occiput, arriving in crops; tufting of three to five hairs may already be visible.
2. Plaque / active. Lesions coalesce into boggy, crusted, actively pustular plaques with fully developed tufted folliculitis (8 to 15 hairs per opening); an active advancing edge surrounds a central zone of evolving scar.
3. Late / cicatricial (burnt-out). Smooth, shiny, atrophic, hairless scalp devoid of follicular markings; a few residual tufts may smoulder at the periphery. The scarring is permanent.[1]

Follicular occlusion kinship. FD belongs to the same family as hidradenitis suppurativa, dissecting cellulitis of the scalp, acne conglobata, and pilonidal sinus — and acne keloidalis nuchae is increasingly grouped with them. A single patient may wear two or more at once (most often FD with dissecting cellulitis or AKN), so consistently that some argue they are one follicular-destructive process expressed at different sites.[5]

[1]

Who you will meet — and what they carry in their nose

FD is uncommon but not rare, and the patient in front of you is usually a young adult man of colour with a staphylococcal saddle on his scalp.[4]

Run the demographic profile on autopilot:[1][4]

• Age: onset typically 20 to 40 years; paediatric and elderly cases are reported but unusual.[10]
• Sex: slight male predominance (about 1.5 to 2:1); women are increasingly recognised.
• Ethnicity and skin type: over-represented in skin of colour (Fitzpatrick IV-VI) — African, South Asian, and Hispanic ancestry — linked to hair-shaft geometry, follicular density, sebum composition, and higher S. aureus nasal carriage.
• Site of onset: scalp vertex and occiput most commonly; rare extra-scalp spread to beard, axillae, pubic area, and gluteal cleft.[1]

Risk factors — and the one that matters most.[1]

• S. aureus nasal and scalp carriage is the single strongest associated factor; carriers relapse more often and benefit from decolonisation.[8]
• Follicular occlusion tendency — coexisting dissecting cellulitis, hidradenitis, AKN, or nodulocystic acne implies a shared occlusion-driven pathology.[5]
• Friction and trauma — tight headgear, helmets, vigorous scratching, harsh chemical relaxers, tight braiding — increase follicular damage and staphylococcal entry.
• Immunosuppression — HIV, transplant recipients, patients on biologics may develop refractory or atypical neutrophilic folliculitis overlapping FD; severe, paediatric, or multi-site disease warrants an immunodeficiency work-up.
• Seborrhoeic and atopic background — increased sebum and an altered scalp microbiome favour S. aureus overgrowth.[8]
• Genetic predisposition — rare familial clusters; severe early-onset disease should prompt thoughts of STAT3 gain-of-function and Hyper-IgE (Job) syndrome, both of which produce refractory staphylococcal folliculitis with scarring.[1]

[1]

Why the follicle dies — the four-step cascade to permanent scar

FD is a neutrophil-mediated follicular-destructive process with four linked steps — and the last one is irreversible.[1][2][8]

Step 1 — Occlusion and S. aureus colonisation. Keratin and altered sebum obstruct the infundibulum, creating an anaerobic niche that favours S. aureus. The FD scalp microbiome shows reduced diversity and enrichment of biofilm-forming Staphylococcus and Corynebacterium.[8]

Step 2 — Abnormal neutrophilic response. S. aureus superantigens (enterotoxins A, B, C, and TSST-1) drive polyclonal T-cell activation and a florid neutrophilic infiltrate that is disproportionate and persistent. The host response — not the organism — is the proximate destroyer, which is why antistaphylococcal monotherapy so often fails: the inflammatory machinery is already self-sustaining.[2][8]

Step 3 — Follicular wall rupture and tufting. Neutrophil elastase and matrix metalloproteinases destroy the epithelial walls of adjacent follicles, fusing them into one dilated common infundibulum. The surviving shafts from each contributing follicle then emerge together through that single enlarged opening — the tufted folliculitis sign, 5 to 20 hairs per opening.[3]

Step 4 — Stem-cell destruction and fibrosis. Inflammation targets the follicular stem cells of the bulge region (the arrector pili insertion). Once they are gone the follicle cannot regenerate, and dense collagenous scar replaces it. This is why the alopecia is permanent: successful treatment halts further loss but regrows nothing in established scar.[1]

Why tufting is pathognomonic. A tuft demands the simultaneous destruction and fusion of several adjacent follicular walls — unique to a neutrophilic, follicle-rupturing process. Lymphocytic scarring alopecias destroy follicles one at a time and never tuft; non-scarring folliculitides do not destroy walls at all. A single tuft at the bedside is diagnostic.[3]

Biofilm is why it comes back. S. aureus inside FD lesions forms biofilm on the hair shaft and within the dilated infundibulum, shielding bacteria from antibiotics and from immunity. That is the biological basis for the chronicity, the high relapse rate, and the non-negotiable need for combination therapy that can penetrate biofilm and prevent resistance.[8]

The overlap is anatomical, not pathological. FD, dissecting cellulitis, and AKN all show follicular occlusion, neutrophilic rupture, and granulomatous fibrosis on histology; they differ only in where they sit (FD = vertex pustules and tufts; DCS = boggy nodules and sinus tracts; AKN = nape keloidal papules). Doche's retrospective series found AKN and FD coexisted in a substantial proportion of patients, backing a shared follicular-destructive process.[5]

The burning edge — read the rim, mourn the centre

At any moment in active FD there is a central zone of burnt-out scar ringed by a rim of active inflammation. Treat the rim; mourn the centre.[1]

Lesion morphology, in the order you meet it:[1][4]

• Follicular papules and pustules in crops on an erythematous base; pustules are small (2 to 5 mm), yellow, often pierced by a central hair.
• Honey-coloured crusting overlying active pustules.
• Tufted folliculitis — clusters of 5 to 20 shafts from one dilated opening, the doll's hair sign, ringed by an erythematous, often boggy halo.
• Progressive scarring alopecia — smooth, shiny, atrophic, hairless scalp devoid of follicular markings, pale centrally with an active erythematous pustular advancing edge.[1]

Distribution. Begins on the scalp vertex (most common) and occiput, spreading centrifugally. Extra-scalp involvement (beard, moustache, axillae, pubic area, gluteal cleft) is rare but recognised.[1]

The burning edge — a consultant confession. I teach every registrar to map the scalp into two zones before prescribing anything. The active (burning) edge — erythema, pustules, crusting, fresh tufts, positive hair-pull — is the only tissue left worth saving. The burnt-out centre is smooth, shiny, hairless, and will stay that way whatever you do. Aim every drug at the rim; spend no effort trying to resurrect the centre.[1]

Symptoms — and the one that patients hide.[1]

• Pain, burning, tenderness in active lesions, often disproportionate to what you see.
• Pruritus of variable severity.
• Discharge of pus or serosanguineous fluid from pustules and boggy areas.
• Cosmetic and psychological distress — visible vertex hair loss is a major quality-of-life injury; depression and anxiety are significantly more common in scarring than non-scarring alopecia.[9]

Atypical presentations — the ones that bend the rule.[10]

• Paediatric FD — rare; identical to adult disease, but severe or recurrent paediatric FD begs the question of underlying immunodeficiency (Hyper-IgE).
• Immunosuppressed / HIV — more extensive, more refractory, may overlap eosinophilic folliculitis; biopsy is mandatory.
• Keloidal FD (skin of colour) — the burnt-out phase forms keloidal or hypertrophic plaques rather than atrophic scar, especially on nape and occiput, blurring the line with AKN.
• Generalised / multi-site FD — simultaneous scalp, beard, and pubic involvement suggests follicular occlusion syndrome; screen for HS, dissecting cellulitis, and acne conglobata.[1]

Pus versus no pus — the bedside fork

Sort the differential the way the biopsy does: the neutrophilic scarring alopecias first, the lymphocytic ones next, then the non-scarring mimics that have not scarred yet.[2][4][7]

[1]

Discriminator line: tufts and pustules on the vertex = FD; boggy sinus tracts = dissecting cellulitis; keloidal papules on the nape = AKN; perifollicular scale and no pus = lymphocytic.[5]

FD versus dissecting cellulitis — three separating features.[1]

1. FD = follicular pustules with tufted hairs in a relatively flat plaque; DCS = boggy, fluctuant nodules and abscesses.
2. FD has no sinus tracts; DCS is defined by interconnecting sinus tracts discharging pus.
3. FD favours the vertex; DCS favours vertex AND occiput with larger confluent boggy plaques and stronger ties to the full occlusion tetrad.[5]

FD versus acne keloidalis nuchae — three separating features.[1]

1. FD = scalp vertex; AKN = nape of neck and lower occiput only.
2. FD = pustules and doll's-hair tufts; AKN = firm keloidal papules and plaques (foreign-body granuloma to ingrown hair).
3. AKN is essentially confined to young men of African descent with tightly curled hair; FD is broader.[5]

[7]

The tuft is the diagnosis — confirm it at the bedside

One unequivocal tuft, in the right clinical context, confirms folliculitis decalvans. Do not wait for the biopsy.[3]

Inspect the vertex for clusters of 5 to 20 shafts emerging from a single dilated opening; the surrounding skin is erythematous and may be crusted or pustular. The single most useful bedside manoeuvre in scarring alopecia costs nothing and decides the day.[3]

Map activity against scar — two zones, opposite prognoses.[1]

• Active (burning) edge — erythema, pustules, crusting, fresh tufting, positive hair-pull (anagen hairs exit easily and painlessly). This is the tissue that will scar next if you do nothing.
• Burnt-out centre — smooth, shiny, atrophic, hairless, no follicular markings, no erythema, negative hair-pull. This will not recover, whatever you prescribe.[1]

Trichoscopy — the four signs to confirm.[6][7]

• Tufted hairs — 5 to 20 shafts from one opening (diagnostic).
• Perifollicular pustules and yellow-orange crusts.
• Perifollicular hyperkeratosis — tubular scaling encircling emerging tufts.
• Empty follicles and absent openings in scarred zones; low-density random vessels, in contrast to the peripilar sign of LPP.[1]

Hair-pull test. Grasp roughly 50 hairs at the active margin and pull firmly; extraction of more than a few anagen hairs marks active disease. In burnt-out scar the pull is negative.[1]

Examine the rest of the body — the occlusion sweep. Look for nape keloidal papules (AKN), axillary and groin sinus tracts (hidradenitis), nodulocystic face, chest, and back acne (acne conglobata), and a natal-cleft sinus (pilonidal). Finding any of them confirms the spectrum and changes management.[5]

Document severity the same way each visit. Serial photographs (same lighting, same angle, vertex and occiput), a ruler on the active edge, and a percentage-scalp-area estimate give objective tracking of response in a disease where "I think it is a bit better" is not good enough.[1]

Swab, scrape, scope, slice — in that order

Diagnosis is clinical, confirmed at the bedside by the tuft; investigations exist to exclude mimics and to choose the antibiotic.[1][2]

Bacterial culture and sensitivity. Swab — or, better, fine-needle-aspirate — a fresh pustule. S. aureus grows in roughly 70%; always request MRSA screening so empirical therapy can be adjusted. A nasal swab identifies carriers who benefit from decolonisation (mupirocin nasal ointment and chlorhexidine body wash) to cut relapse.[8]

Fungal studies — the test you must not skip. KOH and fungal culture are mandatory whenever tinea or kerion is plausible (children, animal contact, boggy plaque, lymphadenopathy). Brush-scalp or pulled-hair culture beats surface swab. Send before any corticosteroid — a steroid-soaked kerion scars, turns culture-negative, and mimics FD for months.[1]

Trichoscopy. Non-invasive confirmation, and the cleanest way to separate FD from the lymphocytic scarring alopecias, which show peripilar white-grey halos and perifollicular hyperkeratosis without pustules or tufting.[6]

Scalp biopsy — site it like a surgeon. Punch two sites: the active advancing edge (a 4-mm punch through a fresh pustule and its erythema) and the burnt-out centre (to document the extent of scarring). The burnt-out centre alone yields non-specific fibrosis and misses the diagnosis.[2][4]

• Early / active histopathology: dense perifollicular neutrophilic infiltrate around infundibulum and isthmus; follicular rupture with extruded keratin and hair-shaft fragments; admixed lymphocytes, plasma cells, and foreign-body giant cells; perifollicular abscess.
• Late / burnt-out histopathology: loss of sebaceous glands, perifollicular concentric ("onion-skin") fibrosis, replacement of follicular units by dense collagen, and a reduced total follicle count. The interfollicular epidermis is normal or atrophic.
• The neutrophilic infiltrate is the single most important discriminator from the lymphocytic scarring alopecias.[1]

Direct immunofluorescence. Send when DLE is in the frame (well-demarcated scaly plaques, conchal involvement, photosensitivity). DLE shows granular IgG, IgM, and C3 along the dermo-epidermal junction (the lupus band); FD is negative.[7]

Baseline bloods before systemic therapy. Full blood count, liver function tests, and urea and electrolytes before rifampicin plus clindamycin, isotretinoin, or dapsone. Check G6PD before dapsone. Pregnancy test (hCG) before isotretinoin or tetracyclines. HIV serology if risk factors or an atypical, refractory course.[1]

First-visit triage — three urgent scenarios

FD is chronic, not an emergency — but three presentations at the first visit cannot wait for the routine pathway.[1]

The three urgent scenarios.[1]

• Severe pain or constitutional symptoms with an acutely boggy, fluctuant plaque — aspirate or incise and drain any abscess; send pus for culture.
• Suspected squamous cell carcinoma in a chronic FD scar — a non-healing ulcer, proliferative nodule, rapid growth, or new pain. Urgent 4-mm punch biopsy; do not assume it is a flare.
• Rapidly progressive scarring with active pustules despite topical therapy — start definitive rifampicin plus clindamycin without further delay. Every extra week of active inflammation destroys more follicles permanently.[1]

Empirical therapy at the first visit — a bridge, not a cure. Swab the pustules, screen for MRSA, and start an empirical antistaphylococcal bridge — oral flucloxacillin 500 mg four times daily (or, in MRSA-positive settings, doxycycline 100 mg BD or clindamycin 300 mg QDS) for one to two weeks — while you arrange definitive combination therapy. Make sure the patient understands this is a holding measure, not the treatment.[1]

Counselling at diagnosis — non-negotiable, and do it in the first ten minutes.[1]

1. The disease is chronic and relapsing; the goal of treatment is to halt further scarring, not to regrow hair in established scar.
2. Scarring is permanent; early aggressive treatment prevents further follicular destruction.
3. Combination systemic therapy is required; monotherapy breeds resistance and relapse.
4. Psychological support is part of the prescription — scarring alopecia carries a significantly elevated risk of depression and anxiety; offer counselling, a support group, and cosmetic camouflage or wig referral.[9]

When to suspect immunodeficiency. Severe, recurrent, multi-site, or paediatric FD warrants screening for Hyper-IgE (Job) syndrome and STAT3 gain-of-function: serum IgE, eosinophil count, and genetic testing if the characteristic facies, eczema, pneumonia, or skeletal abnormalities coexist.[1]

Rifampicin plus clindamycin, never alone — the regimen that owns the viva

There is no randomised trial in FD; the evidence is case series and expert opinion. But one regimen is consistently the most effective, and it is first-line.[1][2]

Management is a stepwise escalation driven by activity and response:[1]

Step 1 — Topical therapy (mild, localised disease, and adjunct throughout).[1]

• Topical corticosteroids: clobetasol propionate 0.05% lotion or foam, or betamethasone dipropionate 0.05%, BD to active edges for up to 4 weeks, then tapered.
• Topical antibiotics: clindamycin 1% lotion or erythromycin 2% solution, BD.
• Antiseptic and keratolytic shampoos: ketoconazole 2% twice weekly (hits Malassezia and S. aureus); chlorhexidine 4% wash daily during flares.
• Mupirocin 2% nasal ointment BD for 5 days each month for documented S. aureus nasal carriers, with chlorhexidine body wash — reduces relapse.[1]

Step 2 — First-line systemic: the rifampicin plus clindamycin combination.[1]

[1]

Step 3 — Second-line systemic agents (refractory, relapsing, or contraindicated combination).[1][2]

• Oral isotretinoin 0.5 mg/kg/day for 4 to 6 months (some escalate to 1 mg/kg/day). Cuts sebum and occlusion; particularly useful when FD overlaps dissecting cellulitis or acne conglobata. Contraception is mandatory (teratogen); monitor lipids and LFTs; avoid concurrent tetracyclines (benign intracranial hypertension).
• Dapsone 50-150 mg daily — anti-neutrophilic via myeloperoxidase inhibition. Check G6PD before starting; monitor haemoglobin and methaemoglobin at 4 weeks and monthly; counsel for haemolysis, especially in Mediterranean, African, or South-East Asian ancestry.
• Oral tetracyclines — doxycycline 100 mg BD or lymecycline 408 mg daily; mainly anti-inflammatory (MMP inhibition) and best for long-term maintenance after rifampicin plus clindamycin. Avoid in pregnancy and in children under 8 years (tooth discolouration).
• Oral zinc sulphate 400 mg daily — small series suggest benefit in refractory disease via anti-inflammatory and anti-androgenic effects.[1]

Step 4 — Intralesional therapy.[1]

• Triamcinolone acetonide 5-10 mg/mL (up to 40 mg/mL for keloidal or hypertrophic variants), 0.05-0.1 mL per site into active inflammatory nodules and plaques every 4 to 6 weeks. Rapidly damps perifollicular inflammation; useful for symptomatic, painful, or cosmetically distressing lesions.[1]

Step 5 — Physical and procedural therapy.[1]

• Laser hair removal — long-pulsed Nd:YAG 1064 nm is the device of choice in skin of colour (Fitzpatrick IV-VI); diode and alexandrite are alternatives in lighter skin. A course of 6 to 10 sessions cuts follicular density, abolishes tufting, and lowers relapse by removing the substrate for inflammation. Nd:YAG is safest in dark skin because its longer wavelength bypasses epidermal melanin.
• Photodynamic therapy (PDT) with MAL or ALA plus red light — case series show benefit in refractory FD; the mechanism is antibacterial and immunomodulatory.[1]

Step 6 — Surgery (rare).[1]

• Excision with primary closure or grafting of a small, stable, burnt-out plaque is occasionally used for cosmesis — but wide recurrence is the rule if you excise during active disease. Scalp reduction is historical and largely abandoned.[1]

Maintenance therapy — the part everyone forgets.[1]

• Long-term topical clindamycin 1% lotion or erythromycin 2% solution, BD to active areas.
• Low-dose oral doxycycline 40 mg daily (sub-antimicrobial) for anti-inflammatory maintenance.
• Ketoconazole 2% / chlorhexidine 4% shampoo twice weekly.
• S. aureus decolonisation in carriers (mupirocin nasal and chlorhexidine body wash).
• Serial photography every 3 to 6 months to catch relapse early.[1]

[1] [1]

When the textbook case bends — children, dark skin, the immunosuppressed

A patient with tufting has FD until proved otherwise — but bend the plan for the child, the keloid-prone scalp, and the immunosuppressed.[3]

Paediatric folliculitis decalvans. Rare; presentation is identical to adult disease, but the dosing and the differential shift:[10]

• Weight-based dosing: rifampicin 15-20 mg/kg/day (max 600 mg/day) in two divided doses; clindamycin 8-25 mg/kg/day in three to four divided doses.
• Avoid tetracyclines under 8 years (tooth discolouration) and avoid isotretinoin in young children except under specialist guidance.
• Investigate immunodeficiency (Hyper-IgE, STAT3) when disease is severe, recurrent, or accompanied by eczema, pneumonia, or skeletal anomalies.[1]

Follicular occlusion overlap. When FD coexists with dissecting cellulitis, hidradenitis, AKN, or acne conglobata, treat the whole spectrum. Oral isotretinoin is the one agent that crosses every member of the spectrum and is often preferred when overlap is present; rifampicin plus clindamycin still handles the FD component.[5]

Skin of colour — keloidal FD. In Fitzpatrick IV-VI skin the burnt-out phase may form keloidal or hypertrophic plaques rather than atrophic scar, particularly on nape and occiput, blurring the boundary with AKN. Add intralesional triamcinolone 10-40 mg/mL into keloidal plaques and prefer Nd:YAG 1064 nm for laser epilation (safest in dark skin). Post-inflammatory hyperpigmentation is a major cosmetic issue; sun protection and hydroquinone-based camouflage help.[5]

Immunosuppressed / HIV-associated neutrophilic folliculitis. In HIV or transplant recipients, an atypical papulopustular eruption on scalp and trunk may mimic or coexist with FD. Biopsy with bacterial, fungal, and mycobacterial cultures is mandatory; eosinophilic folliculitis (Ofuji) is a key mimic needing different therapy (topical corticosteroids, phototherapy, anti-IL-4/13). Antiretroviral optimisation is central.[1]

End-stage / pseudopelade-like FD. A long-standing plaque may evolve into a clinically burnt-out, non-inflammatory, smooth, scarred patch indistinguishable from pseudopelade of Brocq. No active treatment helps here; management is cosmetic camouflage and surveillance for squamous cell carcinoma.[1]

The traps that scar the patient and the doctor

Most FD morbidity is preventable — and most of it is preventable by not making six named errors.[1]

Complications.[1]

• Permanent scarring alopecia — the principal complication; once scarred, hair does not regrow.
• Keloidal or hypertrophic scarring in skin of colour.
• Secondary bacterial infection and, rarely, cellulitis of the scalp.
• Squamous cell carcinoma (Marjolin's ulcer) in chronic cicatricial plaques — rare but reported; any non-healing ulcer, proliferative nodule, or persistent pain in a long-standing scar mandates biopsy.
• Psychological morbidity — depression, anxiety, body-image disturbance, social withdrawal; psychiatric comorbidity is significantly higher in scarring than non-scarring alopecia.[9]
• Drug adverse effects — rifampicin hepatotoxicity and interactions; clindamycin C. difficile colitis; isotretinoin teratogenicity, dryness, dyslipidaemia; dapsone haemolysis and methaemoglobinaemia.[1]

The classic traps — six errors, each one preventable.[1]

• Treating FD as simple staphylococcal folliculitis with a short course of flucloxacillin — relapse is inevitable, because the neutrophilic, biofilm-driven, follicular-destructive process is untouched.
• Using monotherapy — single-antibiotic regimens (rifampicin alone or clindamycin alone) drive rapid resistance and near-universal relapse.
• Missing tinea or kerion by starting corticosteroid before sending fungal culture — converts a treatable infection into a scarring, culture-negative mimic.
• Biopsying the burnt-out centre only — yields non-specific fibrosis and misses the diagnostic neutrophilic infiltrate; always biopsy the active advancing edge.
• Confusing FD with a lymphocytic scarring alopecia — leads to corticosteroid-based regimens that do not address the neutrophilic driver.
• Forgetting rifampicin's CYP3A4 induction — contraceptive failure, warfarin under-anticoagulation, calcineurin-inhibitor under-exposure.[1]

[1]

Chronic, relapsing, permanent — set the expectation on day one

Tell the patient the truth on the first visit: this is a chronic, relapsing disease in which scarring is permanent, and the realistic goal is to halt further loss — not to reverse it.[1]

The disease smoulders over years to decades, with episodes of active pustular inflammation punctuated by quiescent periods; each active episode converts more scalp into permanent scar.[1]

Response to rifampicin plus clindamycin. Roughly 50-70% of patients achieve a durable remission after a single 10 to 12 week course; relapse, when it happens, usually responds to a repeat course or to escalation to isotretinoin or dapsone.[1]

Cosmetic and quality-of-life burden. Visible scarring on the vertex is a major cosmetic and psychological load. A substantial minority need cosmetic camouflage (spray-on hair-fibre concealers, scalp micropigmentation), a wig or hairpiece, or surgical reconstruction (excision of a small stable plaque with primary closure, or follicular unit extraction into burnt-out scar — though transplanted follicles can re-activate disease and the failure rate is significant).[9]

Hair transplantation in FD scar. Controversial. Consider only when disease has been quiescent for at least 6 to 12 months on no active therapy, and even then accept a real risk of koebnerisation and disease reactivation. Most surgeons will not transplant into actively inflamed FD.[1]

Follow-up plan.[1]

• Review at 4 weeks of combination therapy (LFTs, adherence, response), at the end of therapy (12 weeks), then 3-monthly for the first year and 6 to 12-monthly lifelong.
• Serial photography at each visit to catch relapse early.
• Maintenance topical therapy for at least 6 to 12 months after remission.
• Patient education on the relapsing nature, the need to report any new pustule promptly, and the irreversibility of established scar.[1]

Pregnancy, age, and polypharmacy — where the regimen bends

The first-line combination bends in three populations: the child, the pregnant woman, and the patient on an interacting drug.[1]

Paediatric.[10]

• Weight-based dosing: rifampicin 15-20 mg/kg/day in two divided doses (max 600 mg/day); clindamycin 8-25 mg/kg/day in three to four divided doses.
• Avoid tetracyclines under 8 years (permanent tooth discolouration) and avoid doxycycline under 12 years.
• Avoid isotretinoin in prepubertal children except under specialist guidance.
• Screen for immunodeficiency (Hyper-IgE, STAT3 gain-of-function) when disease is severe, recurrent, or accompanied by eczema, pneumonia, coarse facies, or skeletal anomalies.[1]

Pregnancy and breastfeeding.[1]

• SAFE: topical clindamycin, erythromycin, mupirocin, ketoconazole shampoo, and low- to mid-potency topical corticosteroids.
• CONTRAINDICATED: isotretinoin (severe teratogen) and tetracyclines (doxycycline, lymecycline — tooth and bone effects in the fetus); avoid rifampicin unless essential (used for tuberculosis in pregnancy, but the FD indication rarely justifies it).
• Dapsone is generally avoided in the third trimester (theoretical neonatal haemolysis); check G6PD if used.
• Intralesional triamcinolone is acceptable for focal symptomatic lesions.[1]

Elderly and polypharmacy — rifampicin is the hazard. The principal concern is rifampicin's potent CYP3A4 induction. Screen these interactions before starting:[1]

• Warfarin and DOACs — rifampicin markedly lowers anticoagulant levels; intensify INR monitoring or switch the DOAC.
• Oral contraceptive pill — contraceptive failure; counsel a barrier method.
• Statins (especially simvastatin, atorvastatin) — reduced efficacy; recheck lipids.
• Calcineurin inhibitors (ciclosporin, tacrolimus) — sub-therapeutic levels in transplant recipients; close monitoring.
• Anticonvulsants and sulfonylureas — altered levels.
• Clindamycin adds C. difficile risk in the elderly — counsel about diarrhoea.[1]

Skin of colour (Fitzpatrick IV-VI). Keloidal tendency in the burnt-out phase; prominent post-inflammatory hyper- and hypopigmentation. Prefer Nd:YAG 1064 nm over alexandrite or diode (deeper penetration, less epidermal melanin absorption, lower dyspigmentation risk). Test-patch any laser before full treatment.[5]

Immunocompromised / HIV. Lower the threshold for biopsy and culture to exclude infective mimics (eosinophilic folliculitis, dermatophytic folliculitis of Majocchi, bacterial and mycobacterial folliculitis). Optimise antiretrovirals; confirm biopsy-proven FD before committing to prolonged rifampicin plus clindamycin.[1]

No RCTs, two continents — why the evidence is thin but consistent

The evidence base for FD therapy is weak in method but remarkably consistent in conclusion: no randomised trial exists, and the rifampicin plus clindamycin combination is still first-line.[1][2]

The largest synthesis. The systematic review by Rambhia and colleagues (JAAD 2019) pooled case series and reports and concluded that the rifampicin plus clindamycin combination is the most consistently effective regimen, with isotretinoin, dapsone, and laser as alternatives for refractory disease. Subsequent narrative reviews (Svara, 2026) reach the same conclusion.[1]

Emerging targets — still case-report grade. Svara and colleagues survey the next tier: anti-TNF (adalimumab, infliximab), anti-IL-17 (secukinumab), anti-IL-1 (anakinra), and JAK inhibitors (baricitinib, tofacitinib). All are currently at case-report level only, with no trial-grade evidence.[2]

The cohort evidence. Zorlu and colleagues' 15-year tertiary series of 109 primary cicatricial alopecias found the neutrophilic group (FD and dissecting cellulitis) the largest, reinforcing FD's place as a major cause of scarring alopecia in specialist practice.[4]

The overlap evidence. Doche and colleagues' retrospective series showed AKN and FD coexisted in a substantial proportion of patients, supporting one follicular-destructive process expressed at different sites.[5]

The microbiome evidence. The scalp-microbiome literature demonstrates reduced diversity and enrichment of biofilm-forming staphylococci and corynebacteria in FD — the biological rationale for combination antibiotic therapy and antiseptic shampoos.[8]

Cause, coloniser, or bystander? Whether S. aureus is the primary pathogen, a secondary coloniser aggravating an innate-immune defect, or an innocent bystander is unresolved. The clinical implication is clear: antibiotics alone are insufficient — anti-inflammatory and physical measures (laser) are needed to break the self-sustaining inflammatory loop.[1]

Regional deltas — same disease, different starting points.[1]

[1] [1] [1]

Why the evidence base is weak — and what would fix it. FD is rare (no single centre accrues enough patients for an RCT), there is no validated outcome measure, the disease is relapsing-remitting (which confounds short-term assessments), and the most effective regimen cannot easily be blinded. Progress will need multicentre registries.[1]

Exam pearls — the ten facts that own the viva

[1] [1]

Ward-round test — four stems, thirty seconds each

Stem 1 — the man from the top of the topic (answer)

The 34-year-old with eighteen months of vertex pustules, four failed courses of flucloxacillin, smooth scarring, and visible tufts of a dozen hairs from single openings. What is the diagnosis, the cell on biopsy, and the first-line regimen with its duration?[1][3]

Model: Folliculitis decalvans (Quinquaud disease) — a primary neutrophilic cicatricial alopecia, confirmed by the pathognomonic tufted folliculitis. Biopsy of the active edge shows a perifollicular neutrophilic infiltrate with follicular rupture. First-line systemic therapy is rifampicin 300 mg BD plus clindamycin 300 mg BD for 10 to 12 weeks — always as a combination, because monotherapy breeds rifampicin resistance. Flucloxacillin failed because it cannot reach biofilm-embedded organisms and does not switch off the neutrophilic driver.[1][2]

Stem 2 — the boggy child before the steroid (answer)

A 7-year-old returns from a farm with a boggy, pustular, tender scalp mass, cervical lymphadenopathy, and hair loss. The registrar has prescribed oral flucloxacillin and is about to add an intralesional corticosteroid "to settle the inflammation". What must happen first?[7]

Model: Stop. Send KOH and fungal culture before any corticosteroid. This is kerion — an inflammatory tinea capitis — until proved otherwise (child, animal exposure, lymphadenopathy, boggy plaque). A steroid into a kerion converts a treatable infection into a quiet, culture-negative, scarring mimic. Start oral antifungal therapy (griseofulvin or terbinafine, by weight) once the sample is taken; steroids are not the first move.[7]

Stem 3 — the relapse after one antibiotic (answer)

Your patient completed ten weeks of rifampicin 300 mg BD alone (the GP read "rifampicin" and stopped the clindamycin at week two because of diarrhoea). The pustules settled, then roared back within a month. What went wrong, and what do you do now?[1]

Model: Two errors. Monotherapy drives rifampicin resistance — clindamycin is not a sidekick, it is the partner that prevents it; stopping it forfeits the rationale. And clindamycin-related diarrhoea should prompt C. difficile testing and a switch, not a quiet abandonment of the combination. Now: re-culture, confirm the organism is still sensitive, and give a proper rifampicin 300 mg BD plus clindamycin 300 mg BD combination for a full 10 to 12 weeks, with LFT monitoring and a documented diarrhoea plan. Escalate to isotretinoin or dapsone if the second course fails.[1][2]

Stem 4 — the ulcer in the old scar (answer)

A 62-year-old with a twenty-year history of burnt-out FD on the vertex presents with a non-healing ulcer and new pain inside the scar over three months. The team calls it a "flare". Your move?[1]

Model: This is not a flare — it is squamous cell carcinoma (Marjolin's ulcer) until the biopsy says otherwise. A non-healing ulcer, proliferative nodule, or new pain in a chronic cicatricial plaque mandates an urgent 4-mm punch biopsy. Do not reach for more antibiotics or steroids first. Marjolin's ulcer is rare but reported in long-standing FD scars, and the cost of missing it is a delayed cancer diagnosis.[1]

References

1. [1]Rambhia PH, Conic RRZ, Murad A, et al. Updates in therapeutics for folliculitis decalvans: A systematic review with evidence-based analysis J Am Acad Dermatol, 2019.PMID 30092322
2. [2]Svara F, Bortone G, Ambrosio L, et al. Diagnostic Challenges and Treatment Strategies in Neutrophilic Cicatricial Alopecias: A Narrative Review from Conventional Therapies to New Therapeutic Targets Life (Basel), 2026.PMID 42195390
3. [3]Saleh HM, Sathe NC Tufted Hair Folliculitis 2026.PMID 28613486
4. [4]Zorlu Ö, Albayrak H, Aytekin S Clinical features of 109 patients with primary cicatricial alopecia: a 15-year retrospective study Acta Dermatovenerol Alp Pannonica Adriat, 2026.PMID 41915583
5. [5]Doche I, Coelho EQ, Quaresma MV, et al. Acne keloidalis nuchae and folliculitis decalvans: same process affecting the follicle or coexisting diseases? A retrospective study Int J Dermatol, 2019.PMID 31241169
6. [6]Pirmez R The dermatoscope in the hair clinic: Trichoscopy of scarring and nonscarring alopecia J Am Acad Dermatol, 2023.PMID 37591567
7. [7]Alessandrini A, Bruni F, Piraccini BM, et al. Common causes of hair loss - clinical manifestations, trichoscopy and therapy J Eur Acad Dermatol Venereol, 2021.PMID 33290611
8. [8]Shah RR, Larrondo J, Dawson T, et al. Scalp microbiome: a guide to better understanding scalp diseases and treatments Arch Dermatol Res, 2024.PMID 39073596
9. [9]Baker NJ, Alomary SA, Ogunleye T, et al. Risk of Psychiatric Comorbidities in Non-Scarring Versus Scarring Alopecia: A Retrospective Cohort Study J Cutan Med Surg, 2026.PMID 41925130
10. [10]Motsios D, Sotiropoulou K, Karabarba S, et al. Comprehensive Case Report on Folliculitis Decalvans in a Pediatric Patient Acta Dermatovenerol Croat, 2025.PMID 42370657